AUTHOR=Nguyen Nam Khoa , Wang Juan , Liu Dongping , Hwang Byung Kook , Jwa Nam-Soo 

TITLE=Rice iron storage protein ferritin 2 (OsFER2) positively regulates ferroptotic cell death and defense responses against Magnaporthe oryzae

JOURNAL=Frontiers in Plant Science

VOLUME=13

YEAR=2022

URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2022.1019669

DOI=10.3389/fpls.2022.1019669

ISSN=1664-462X

ABSTRACT=<p>Ferritin is a ubiquitous iron storage protein that regulates iron homeostasis and oxidative stress in plants. Iron plays an important role in ferroptotic cell death response of rice (<italic>Oryza sativa</italic>) to <italic>Magnaporthe oryzae</italic> infection. Here, we report that rice ferritin 2, OsFER2, is required for iron- and reactive oxygen species (ROS)-dependent ferroptotic cell death and defense response against the avirulent <italic>M. oryzae</italic> INA168. The full-length ferritin OsFER2 and its transit peptide were localized to the chloroplast, the most Fe-rich organelle for photosynthesis. This suggests that the transit peptide acts as a signal peptide for the rice ferritin OsFER2 to move into chloroplasts. <italic>OsFER2</italic> expression is involved in rice resistance to <italic>M. oryzae</italic> infection. <italic>OsFER2</italic> knock-out in wild-type rice HY did not induce ROS and ferric ion (Fe<sup>3+</sup>) accumulation, lipid peroxidation and hypersensitive response (HR) cell death, and also downregulated the defense-related genes <italic>OsPAL1</italic>, <italic>OsPR1-b</italic>, <italic>OsRbohB</italic>, <italic>OsNADP-ME2-3</italic>, <italic>OsMEK2</italic> and <italic>OsMPK1</italic>, and vacuolar membrane transporter <italic>OsVIT2</italic> expression. <italic>OsFER2</italic> complementation in <italic>ΔOsfer2</italic> knock-out mutants restored ROS and iron accumulation and HR cell death phenotypes during infection. The iron chelator deferoxamine, the lipid-ROS scavenger ferrostatin-1, the actin microfilament polymerization inhibitor cytochalasin E and the redox inhibitor diphenyleneiodonium suppressed ROS and iron accumulation and HR cell death in rice leaf sheaths. However, the small-molecule inducer erastin did not trigger iron-dependent ROS accumulation and HR cell death induction in <italic>ΔOsfer2</italic> mutants. These combined results suggest that <italic>OsFER2</italic> expression positively regulates iron- and ROS-dependent ferroptotic cell death and defense response in rice–<italic>M. oryzae</italic> interactions.</p>